Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nitrous oxide withdrawal syndrome in mice was used as an experimental model to examine some of the factors which may play a role in postanesthetic excitation. Predisposition to nitrous oxide withdrawal convulsions as judged by duration of susceptibility was decreased significantly after pretreatment with the cholinesterase inhibitors, physostigmine and galanthamine, or with the opiate receptor blocking agent naloxone. Results are discussed in relation to the central anticholinergic syndrome, endorphin release, and disturbances which follow nitrous oxide anesthesia in humans and animals.
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PMID:The involvement of the central cholinergic and endorphinergic systems in the nitrous oxide withdrawal syndrome in mice. 668 88

The effects of reversible (galanthamine, eserine) and irreversible organophosphate (armine) cholinesterase inhibitors on excitable muscle fibre membrane of the frog involved elongation of the rise and the half-decay time of the AP (galanthamine and eserine), the critical level of depolarization being shifted to a more negative value. Armine decreased the rise and the half-decay time, the critical level of depolarization being shifted to the positive direction; subsequent rising of the threshold often caused blocking of neuro-muscular transmission during the first minutes of the armine action, pretreatment of preparations with galanthamine (eserine) preventing the threshold increase and armine blocking of transmission. Probably mechanism of these drugs action on the membrane channels is discussed. The negative shift of critical level seems to underlie the protective action of galanthamine and eserine in case of poisoning with irreversible cholinesterase inhibitors.
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PMID:[Effect of cholinesterase inhibitors on the electrical excitability of the membrane of frog muscle fiber]. 717 36

Study into migration activity of leukocytes in vitro allowed a conclusion that the inhibitors of cholinesterase, armin, takrin and galanthamine, decrease this function. Low doses of atropine stimulate whereas high ones inhibit the migration of leukocytes. Atropine and armin act like antagonists as regards the action on the biological parameter in question: an adverse action of armin can be prevented by atropine.
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PMID:[Effect of cholinergic preparations on leukocyte migration]. 726 5

We studied the effect of intravenous injection of the cholinesterase inhibitor galanthamine (GAL) in doses from 0.025 to 5.0 mg/kg on electrically evoked field potentials in rat visual cortex. In all the experiments the amplitude of late components of evoked potentials was significantly reduced, while early components remained unaffected. These findings indicate that cortical cells are inhibited by acetylcholine (ACh). Furthermore, combined application of a muscarinic receptor blocker (atropine) and GAL reliably suppressed the effects of galanthamine. These observations suggest that ACh-induced inhibition may be mediated by activation of GABAergic interneurones that possess muscarinic receptors.
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PMID:Effect of the cholinesterase-inhibiting substance galanthamine on evoked visual potentials in rats. 766 Aug 64

Experiments on non-inbred albino mice have demonstrated that aminostigmine is an active reversible centrally active cholinesterase inhibitor close to the properties of physostigmine, but greatly superior to it in its action duration. Clinical examinations of healthy volunteers and patients have shown that aminostigmine-induced inhibition of cholinesterase activity persists 6 hours. The agent have been found to be more highly effective in treating cholin blocker-induced intoxications than galanthamine, which manifests itself in its greater stability of the therapeutical effect achieved and in its higher ability to prevent cardiovascular events occurring in intoxication.
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PMID:[Aminostigmine as a cholinesterase inhibitor and as an agent for treating poisonings by cholinergic blockers]. 769 93

The disappearance kinetics of the acetylcholinesterase inhibitor galanthamine hydrobromide from the gastrointestinal tract of male Wistar rats, 200-250 g, in-situ has been examined. After 30 min the galanthamine loss was 16% in the stomach (pH 2), 54-85% in the duodenum and the successive small intestinal segments (pH 6.8), 43% in the colon and 76% in the rectum. Compared with the other segments, the disappearance rate was higher in the terminal ileum (0.38 x 10(-2) mg cm-1 min) and in the rectum (1.27 x 10(-2) mg cm-1 min). In the proximal jejunum, terminal ileum and rectum the disappearance rate was linearly dependent on the galanthamine dose (range 0.5-4 mg, 2-16 mg kg-1). The results suggest that when administered orally, rapid galanthamine absorption could be expected all over the gastrointestinal tract due mainly to the passive diffusion mechanism.
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PMID:Gastrointestinal loss of galanthamine hydrobromide in rats in-situ. 790 79

The pharmacokinetic of some centrally acting cholinesterase inhibitors that have been used to improve memory in patients with dementia of Alzheimer's type, was compared. The original compound in this class, physostigmine has an elimination half-life of 20-30 min. Galanthamine, tacrine and the metabolite 1-hydroxytacrine (velnacrine) have longer elimination half-lives of 1.6-6 hours mainly due to a larger volume of distribution. The concentration of tacrine in the cerebrospinal fluid (CSF) was less than the average plasma concentration in the dosing interval; a ratio of 0.74. The concentration of 1-hydroxytacrine and other metabolites of tacrine in the CSF were higher than the average concentrations of the compounds in plasma.
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PMID:Pharmacokinetic studies of cholinesterase inhibitors. 812 33

Evidence from animal experiments has suggested that the triggering and maintenance of rapid eye movement (REM) sleep is mainly under the control of cholinergic neurons in the brain stem. Correspondingly, studies in humans have demonstrated that the application of cholinergic agonists or cholinesterase inhibitors provokes an earlier onset of REM sleep. The present study investigated the influence of galanthamine hydrobromide, a reversible cholinesterase inhibitor, on REM sleep regulation in 18 healthy volunteers. After an adaptation night, the subjects were given two doses of galanthamine (10 mg and 15 mg) or placebo at 10 p.m. in a randomized double-blind design. Both doses of galanthamine shortened REM latency (with statistical significance depending on the definition of REM latency used), increased REM density, and reduced slow wave sleep mainly in the first non-REM cycle. Higher doses of galanthamine (15 mg) seem to be accompanied by unwanted side effects that warrant the application of a peripheral antidote. These results are comparable to those for other cholinomimetics and stress the usefulness of galanthamine for pharmacological challenge studies in healthy subjects and depressed patients.
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PMID:Influence of the cholinesterase inhibitor galanthamine hydrobromide on normal sleep. 820 72

The muscarinic antagonist scopolamine (SCOP; 1.0 mg/kg, ip) impaired both the acquisition of a learning task in the Morris water maze (MWM) and choice accuracy in the T-maze reinforced alternation procedure in rats. Acetylcholinesterase inhibitors (AChEIs) have been shown to attenuate these deficits. D-Cycloserine (DCS), a partial agonist at the strychnine-insensitive glycine site on the N-methyl-D-aspartate (NMDA) receptor complex, was investigated for its effects on SCOP-induced dementia in the MWM and T-maze paradigms. Combined administration of SCOP and DCS (3.0, 10.0, or 30.0 mg/kg, ip; 30 min pretreat) significantly reversed SCOP-induced deficits in the T-maze as measured by percentage correct choices. In addition, DCS (3.0 or 10.0 mg/kg, ip) significantly attenuated SCOP-induced deficits in the MWM as measured by latency to find the submerged platform. For comparison, the long-acting acetylcholinesterase inhibitor galanthamine (GAL) was tested in the T-maze (1.25, 2.5, or 5.0 mg/kg, ip) and the MWM (2.5 or 5.0 mg/kg, ip). GAL attenuated SCOP-induced deficits in both learning and memory models similar to DCS. These data suggest that the strychnine-insensitive partial glycine agonist, D-cycloserine, may be efficacious in disease states of central cholinergic hypofunction such as Alzheimer's disease.
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PMID:D-cycloserine attenuates scopolamine-induced learning and memory deficits in rats. 847 82

Galanthamine is an alkaloid found in the bulbs of snowdrops and several Amaryllidaceae plants. At submicromolar concentrations, it inhibits acetylcholinesterase activity, but it is much less potent against butyrylcholinesterase activity. Galanthamine has been used in anaesthetics to reverse neuromuscular paralysis by tubocurarine-like muscle relaxants, but it is a tertiary amine that gets into the brain to cause central effects. Galanthamine is being studied as a possible therapeutic agent in Alzheimer's disease because of its central cholinergic effects. Positive effects have been demonstrated in several learning and memory tests in animals.
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PMID:The pharmacology of galanthamine and its analogues. 860 34


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